Currently prescribed therapeutics for MI patients are designed to reduce hypertrophy via several neurohormonal mechanisms including inhibition of angiotensin II (AngII) and norepinephrine (NE) or increasing the bioavailability of natriuretic peptides (NPs) (Ponikowski et al., 2016), but no drugs have been approved for treating cardiac fibrosis directly. Here, AGT is linked to myocardial infarction.